Hydroxytyrosol, a product from olive oil, reduces colon cancer growth by enhancing epidermal growth factor receptor degradation

2015 ◽  
Vol 60 (3) ◽  
pp. 519-529 ◽  
Author(s):  
Erika Terzuoli ◽  
Antonio Giachetti ◽  
Marina Ziche ◽  
Sandra Donnini
Keyword(s):  
Colon Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Olive Oil ◽  
Growth Factor Receptor ◽  
Cancer Growth ◽  
Epidermal Growth

Nicotine Promoted Colon Cancer Growth via Epidermal Growth Factor Receptor, c-Src, and 5-Lipoxygenase-Mediated Signal Pathway

2003 ◽  
Vol 308 (1) ◽  
pp. 66-72 ◽  
Author(s):  
Yi N. Ye ◽  
Edgar S. L. Liu ◽  
Vivian Y. Shin ◽  
William K. K. Wu ◽  
Jiing C. Luo ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Signal Pathway ◽  
Cancer Growth ◽  
Epidermal Growth

Epidermal growth factor receptor transactivation is required for proteinase-activated receptor-2-induced COX-2 expression in intestinal epithelial cells

2012 ◽  
Vol 303 (1) ◽  
pp. G111-G119 ◽  
Author(s):  
Christina L. Hirota ◽  
France Moreau ◽  
Vadim Iablokov ◽  
Michael Dicay ◽  
Bernard Renaux ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Intestinal Epithelial Cells ◽  
Growth Factor Receptor ◽  
Intestinal Epithelial ◽  
Kinase Signaling ◽  
Epidermal Growth ◽  
Cox 2

Proteinase-activated receptor (PAR)2, a G protein-coupled receptor activated by serine proteinases, has been implicated in both intestinal inflammation and epithelial proliferation. Cyclooxygenase (COX)-2 is overexpressed in the gut during inflammation as well as in colon cancer. We hypothesized that PAR2 drives COX-2 expression in intestinal epithelial cells. Treatment of Caco-2 colon cancer cells with the PAR2-activating peptide 2-furoyl-LIGRLO-NH2 (2fLI), but not by its reverse-sequence PAR2-inactive peptide, for 3 h led to an increase in intracellular COX-2 protein expression accompanied by a COX-2-dependent increase in prostaglandin E2 production. 2fLI treatment for 30 min significantly increased metalloproteinase activity in the culture supernatant. Increased epidermal growth factor receptor (EGFR) phosphorylation was observed in cell lysates following 40 min of treatment with 2fLI. The broad-spectrum metalloproteinase inhibitor marimastat inhibited both COX-2 expression and EGFR phosphorylation. The EGFR tyrosine kinase inhibitor PD153035 also abolished 2fLI-induced COX-2 expression. Although PAR2 activation increased ERK MAPK phosphorylation, neither ERK pathway inhibitors nor a p38 MAPK inhibitor affected 2fLI-induced COX-2 expression. However, inhibition of either Src tyrosine kinase signaling by PP2, Rho kinase signaling by Y27632, or phosphatidylinositol 3 (PI3) kinase signaling by LY294002 prevented 2fLI-induced COX-2 expression. Trypsin increased COX-2 expression through PAR2 in Caco-2 cells and in an EGFR-dependent manner in the noncancerous intestinal epithelial cell-6 cell line. In conclusion, PAR2 activation drives COX-2 expression in Caco-2 cells via metalloproteinase-dependent EGFR transactivation and activation of Src, Rho, and PI3 kinase signaling. Our findings provide a mechanism whereby PAR2 can participate in the progression from chronic inflammation to cancer in the intestine.

Ligand-dependent activation of the epidermal growth factor receptor by secondary bile acids in polarizing colon cancer cells

Surgery ◽  
2005 ◽  
Vol 138 (3) ◽  
pp. 415-421 ◽  
Author(s):  
Nipun B. Merchant ◽  
Christopher M. Rogers ◽  
Bakula Trivedi ◽  
Jason Morrow ◽  
Robert J. Coffey
Keyword(s):  
Colon Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cancer Cells ◽  
Bile Acids ◽  
Growth Factor Receptor ◽  
Colon Cancer Cells ◽  
Epidermal Growth ◽  
Secondary Bile Acids

Lauric acid induce cell death in colon cancer cells mediated by the epidermal growth factor receptor downregulation: An in silico and in vitro study

2019 ◽  
Vol 38 (7) ◽  
pp. 753-761 ◽  
Author(s):  
DL Sheela ◽  
A Narayanankutty ◽  
PA Nazeem ◽  
AC Raghavamenon ◽  
SR Muthangaparambil
Keyword(s):  
Fatty Acids ◽  
Colon Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lauric Acid ◽  
Caprylic Acid ◽  
Growth Factor Receptor ◽  
Capric Acid ◽  
Epidermal Growth

Coconut oil (CO) is enriched with medium chain saturated fatty acids like lauric acid (LA), capric acid and caprylic acid, which are known to have several health benefits. LA, the predominant fatty acid in CO, is reported to possess anticancer activity mediated through oxidative stress-induced apoptosis; however, there is no clear information on its cellular signalling mechanism. The present study screened the anticancer potential of various fatty acids present in CO (capric acid, caprylic acid and LA) using in silico tools such as CDOCKER in Accelrys Discovery Studio by targeting proteins like epidermal growth factor receptor (EGFR), cyclin-dependent kinase and thymidine synthase (TS). The results were further confirmed using cell culture-based studies and quantitative PCR. Among the tested compounds, LA was found to be the most active and showed a higher affinity towards EGFR and TS. Corroborating with these results, LA-induced dose-dependent cytotoxicity towards HCT-15 (human colon cancer), HepG2 (human hepatocellular carcinoma) and Raw 264.7 (murine macrophages) cells exhibiting morphological characteristics of apoptosis. Further, in HCT-15 cells exposed to LA (30 and 50 µg/mL), the expression of EGFR was found to be downregulated by 1.33- and 1.58-fold. The study thus concludes that the anticancer activity of LA may be partially mediated by the downregulation of EGFR signalling and consequent reduction in cell viability through apoptosis. Since EGFR signalling is crucial in cancer cell survival and is a prime target in drug development, the present study has pharmacological significance.

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